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Flow chart of recruited patients

Flow chart of recruited patients

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Subarachnoid haemorrhage (SAH) is associated with long-term disability, serious reduction in quality of life and significant mortality. Early brain injury (EBI) refers to the pathological changes in cerebral metabolism and blood flow that happen in the first few days after ictus and may lead on to delayed cerebral ischaemia (DCI). A disruption of t...

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... Residual nitrite contained in the slices might account for the • NO signal under control conditions ( Figure 3B). In agreement with these results, it has been reported that there is a protective action of nitrite during ischemia and ischemia-reperfusion in several organs, including in the brain [56][57][58], and this protection is attributed to its reduction in • NO. ...
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Nitric oxide (•NO), a diffusible free radical, is an intercellular messenger, playing a crucial role in several key brain physiological processes, including in neurovascular coupling (NVC). In the brain, glutamatergic activation of the neuronal nitric oxide synthase (nNOS) enzyme constitutes its main synthesis pathway. However, when oxygen (O2) supply is compromised, such as in stroke, ischemia, and aging, such •NO production pathway may be seriously impaired. In this context, evidence suggests that, as already observed in the gastric compartment, the reduction of nitrite by dietary compounds (such as ascorbate and polyphenols) or by specific enzymes may occur in the brain, constituting an important rescuing or complementary mechanism of •NO production. Here, using microsensors selective for •NO, we show that nitrite enhanced the •NO production in a concentration-dependent manner and in the presence of ascorbate evoked by N-methyl-D-aspartate (NMDA) and glutamate stimulation of rat hippocampal slices. Additionally, nitrite potentiated the •NO production induced by oxygen-glucose deprivation (OGD). Overall, these observations support the notion of a redox interaction of ascorbate with nitrite yielding •NO upon neuronal glutamatergic activation and given the critical role of NO as the direct mediator of neurovascular coupling may represents a key physiological mechanism by which •NO production for cerebral blood flow (CBF) responses to neuronal activation is sustained under hypoxic/acidic conditions in the brain.
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Background Better outcome prediction could assist in reliable classification of the illnesses in neurological intensive care unit (ICU) severity to support clinical decision-making. We developed a multifactorial model including quantitative electroencephalography (QEEG) parameters for outcome prediction of patients in neurological ICU. Methods We retrospectively analyzed neurological ICU patients from November 2018 to November 2021. We used 3-month mortality as the outcome. Prediction models were created using a linear discriminant analysis (LDA) based on QEEG parameters, APACHEII score, and clinically relevant features. Additionally, we compared our best models with APACHEII score and Glasgow Coma Scale (GCS). The DeLong test was carried out to compare the ROC curves in different models. Results A total of 110 patients were included and divided into a training set (n=80) and a validation set (n = 30). The best performing model had an AUC of 0.85 in the training set and an AUC of 0.82 in the validation set, which were better than that of GCS (training set 0.64, validation set 0.61). Models in which we selected only the 4 best QEEG parameters had an AUC of 0.77 in the training set and an AUC of 0.71 in the validation set, which were similar to that of APACHEII (training set 0.75, validation set 0.73). The models also identified the relative importance of each feature. Conclusion Multifactorial machine learning models using QEEG parameters, clinical data, and APACHEII score have a better potential to predict 3-month mortality in non-traumatic patients in neurological ICU.